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http://purl.uniprot.org/SHA-384/B3ABA14E691A0C7DA6C72FD5EC008A78CE0D64723859DB9C1B064ADFE9563B3E4EF46B6CC7E0F1B66470FAA107DC2B3Fhttp://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Annotation
http://purl.uniprot.org/SHA-384/B3ABA14E691A0C7DA6C72FD5EC008A78CE0D64723859DB9C1B064ADFE9563B3E4EF46B6CC7E0F1B66470FAA107DC2B3Fhttp://www.w3.org/2000/01/rdf-schema#comment"Results demonstrated that TUBB3 mutations impair the interaction of DCC with polymerized TUBB3 in MTs and inhibit netrin-1-induced neurite outgrowth branching and attraction. These results suggest a disease mechanism underlying TUBB3 mutation-associated axon guidance defects: mutations in TUBB3 disrupt engagement of netrin/DCC signaling with MT dynamics resulting in specific defects of netrin-1-mediated axon projection."xsd:string
http://purl.uniprot.org/uniprot/#_68A55E209CFC8152D639A93592D221FA3A199BB2B2B23F4D32A8D771FEBF0001112572A78F30E5230010EB0EC4CECD22http://www.w3.org/1999/02/22-rdf-syntax-ns#subjecthttp://purl.uniprot.org/SHA-384/B3ABA14E691A0C7DA6C72FD5EC008A78CE0D64723859DB9C1B064ADFE9563B3E4EF46B6CC7E0F1B66470FAA107DC2B3F
http://purl.uniprot.org/uniprot/Q3ZCR3http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/B3ABA14E691A0C7DA6C72FD5EC008A78CE0D64723859DB9C1B064ADFE9563B3E4EF46B6CC7E0F1B66470FAA107DC2B3F
http://purl.uniprot.org/uniprot/#_Q3ZCR3-mappedCitation-29382549http://purl.uniprot.org/core/mappedAnnotationhttp://purl.uniprot.org/SHA-384/B3ABA14E691A0C7DA6C72FD5EC008A78CE0D64723859DB9C1B064ADFE9563B3E4EF46B6CC7E0F1B66470FAA107DC2B3F